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CLS 304 > Chapter 9 Kidney Disease > Flashcards

Chapter 9 Kidney Disease Flashcards

1
Q

Diagnosis and screening to determine kidney diseases

A
  • Abnormality in biochemical blood screen
  • functional change in glomerular filtration rate (GFR)
  • abnormality in urinalysis: proteinuria and hematuria
  • systemic disease with renal involvement: diabetes mellitus
  • symptom, physical sign, imaging
  • kidney biopsy
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2
Q

Major types based on where kidney was initially affected

A
  1. Glomerular
  2. Tubular
  3. Interstitial
  4. Vascular
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3
Q

What major type is most often immune related?

A

Glomerular

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4
Q

What major type affects proximal/distal tubules and is a result from toxic or infectious substances

A

Tubular

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5
Q

What major type is damage from neglected UTIs and result from toxic or infectious substances

A

Interstitial

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6
Q

What major type affects blood flow from the heart and reduces renal perfusion?

A

Vascular

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7
Q

Types of glomerular disorders and morphologic changes

A 
Distinct changes/damage:
- immunologic
- non-immunologic
Types:
- primary immunologic
- Secondary to systemic diseases
- hereditary
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8
Q

Immune mediated changes in glomerulus

A
  • Cellular proliferation: increased numbers of endothelial and other cells
  • Leukocyte infiltration
  • glomerular basement membrane thickening: immune complexes and diabetes
  • Hyalinization with sclerosis (scarring)
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9
Q

Clinical features of nephritis vs nephrotic diseases

A
  • Hematuria
  • proteinuria
  • Lipiduria
  • oliguria
  • Azotemia (increased blood urea nitrogen)
  • Edema
  • Hypertension
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10
Q

2 glomerular diseases

A

Nephritic and nephrotic: acute, chronic

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11
Q

Features of nephrotic syndrome

A
  • Onset: insidious
  • Edema: ++++
  • Blood pressure: normal
  • jugular venous pressure:normal/low
  • Proteinuria: ++++
  • Hematuria: may/may not occur
  • red blood cell casts: absent
  • serum albumin: low
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12
Q

Features of nephritic syndrome

A
  • Onset: abrupt
  • edema: ++
  • blood pressure: raised
  • jugular venous pressure: raised
  • proteinuria: ++
  • hematura: +++
  • Red blood cell casts: present
  • serum albumin: normal/ slightly reduced
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13
Q

Cause of nephrotic syndrome

A

Increased permeability of the glomerular due to damage of basal Lamina and podocytes. Massive loss of protein (mostly albumin) in urine

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14
Q

Clinical findings of nephrotic syndrome

A

Pronounced soft and pitting edema and hyperlipidemia

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15
Q

Urinalysis of nephrotic syndrome

A

Cloudy, fat droplets

  • protein > 3.5g/day and 4+ positive on dipstick
  • lipiduria
  • oily
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16
Q

Microscopic findings of nephrotic syndrome

A
  • Oval fat bodies, free fat globes
  • increased renal tubular epithelial cells
  • increased casts: all types, particularly fatty, waxy, and renal well
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17
Q

Cause of acute post streptococcal glomerutonephritis

A

Sudden onset occurs 1-2 weeks after group A beta-hemolytic strep with M protein infection of throat or skin (strep throat)

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18
Q

Clinical findings of acute post streptococcal glomerulonephritis

A

Fever, edema, fatigue, hypertension, Algeria, hematuria

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19
Q

Urinalysis of acute post streptococcal glomerulonephritts

A

Cloudy, red or brown

- protein ( = casts), blood ( increased ASO titer and BUN), leukocyte esterase positive (need to look at in microscopic)

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20
Q

Microscopic findings of acute Post streptococcal glomerulonephritis

A
  • Increased RBCs, often dymorphic
  • Increased WBCs
  • increased renal tubular epithelial cells
  • Increased casts: RBC, hemoglobin, granular
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21
Q
A

Normal glomerulus

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22
Q
A

Post strep glomerulus

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23
Q

Rapidly progressive crescentric (acute nephritic)

A
  • Cellular proliferation in Bowman’s space form crescents: leukocyte infiltration; fibrin deposits; damages to glomerular basement membrane
  • Complication of systemic lupus erythematosis
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24
Q

Minimal change disease (acute nephrotic)

A

Loss of podocyte foot processes; dysfunction of t-cell immunity; follows infections and responsible for most cases of nephrotic syndrome in children; rapid response to steroids

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25
Focal glomerulosclerosis (variable)
Sclerotic damage to limited number of glomeruli with hyaline and lipid deposits and loss of foot processes; focal IgM and C3 deposits. Proteinuria predominant
26
Changes in glomerular membrane and cellular structures
- Results in varying degrees of hematuria and proteinuria - thickening of membrane due to deposits of IgG immune complexes - alteration of cellularity of the capillary walls - IgA deposits on glomerular membrane 1-2 days following a mucosal infection of respiratory, gastro, or urinary tract infection from infectious agents that stimulate IgA - disruption and damage of podocytes
27
Cause of chronic glomerulonephritis
- slow and progressive damage to the glomeruli - leads tow chronic/end stage renal disease - impaired GFR
28
Clinical findings of chronic glomerulonephritis
Edema, azotemia, hypertension, oliguria, hematuria, anemia
29
Urinalysis of chronic glomerulonephritis
Protein > 2.5g/day, blood, leukocyte esterase positive
30
Microscopic findings of chronic glomerulonephritis
- Increased RBCs, often dysmorphic - increased WBCs - increased renal tubular epithelial cells - increased casts: all types, particularly granular, waxy, broad
31
Systemic diseases associated with glomerulonephritis
- Diabetes mellitus - autoimmune disorders: systemic lupus erythematosus (SLE), sjogren syndrome, Berger disease, IgA - amyloidosis - Infections: viral: HIV, HBV bacterial: group A strep, syphilis - malignancies:multiple myeloma
32
Cause of acute tubular necrosis (ATN)
Damage to renal tubular epithelium caused by: - Ischemia due to decreased blood flow and lack of oxygen to RTE cells seen in shock, sepsis, trauma - toxic substances in urine: exogenous (antibiotics, heavy metals, organic solvents, heron, cocaine, poisons) and endogenous (myoglobin and hemoglobin) - can cause oliguria and acute renal failure
33
Urinalysis of acute tubular necrosis (ATN)
Cloudy, red or brown | - protein small, blood positive
34
Microscopic findings of acute tubular necrosis (ATN)
- Increased RBCs, often dysmorphic - increased renal tubular epithelial (RTE) cells - Increased casts: RTE most abundant, hyaline, granular, waxy
35
Tubular dysfunction examples: Fanconi syndrome
Loss of proximal tubular function
36
Tubular dysfunction examples: impaired ability to reabsorb specific substances
- Cystinosis and cystinuria amino acids | - glucose, calcium, bicarbonate, sodium, phosphate
37
Tubular dysfunction examples: renal tubular acidosis
Inability to secrete hydrogen ions so blood is acidic but unable to produce an acid urine
38
Interstitial disorders: UTI
- Most common renal disease - lower urinary tract urethra and bladder: contaminated by fecal, to tight clothes. Most common, + leukocyte esterase and ketones - Upper urinary tract renal pelvis, tubules, interstitium: from antibiotics
39
Interstitial disorders: cystitis
Ascending bacterial infection of bladder
40
Interstitial disorders: urethritis
Infection of urethra
41
Clinical findings of UTI, cystitis, urethntis
Cloudy, odorous | - pH alkaline, protein, blood, leukocyte esterase, nitrite
42
Microscopic findings for UTI, cystitis, urethritis
- Increased RBCs and WBCs - increased transitional epithelium cells - bacteria/yeasts Urine culture for specific ID
43
Cause of pyelonephritis
Infection of upper urinary tract tubules/interstitium | - acute and chronic presentation
44
Clinical findings of pyelonephritis
- Acute sudden onset of lower back pain, urinary frequency, burning, fever, headache, general malaise - recurrent infections leads to chronic and can progress to renal failure - obstructions and bladder/ureters reflux
45
Urinalysis of pyelonephritis
Cloudy, odorous | - protein, blood, leukocyte esterase, nitrite
46
Microscopic findings of pyelonephritis
- Increased WBCs and WBC casts (also granular, waxy, RTE) - increased RBCs - Bacteria Urine and blood cultures
47
Cause of acute interstitial nephritis
Allergic inflammation of renal interstitium followed by inflammation of renal tubules in response to certain medications. Must common cause is acute allograft rejection of a transplanted kidney
48
Clinical findings of acute interstitial nephritis
Sudden onset of renal symptoms, rash, fever develops app. 2 weeks after medication taken
49
Urinalysis of acute interstitial nephritis
Protein, blood, leukocyte esterase
50
Microscopic findings of acute interstitial nephritis
- Increased WBCs with eosinophils - WBC eosinophilic cast may be present - increased RBCS - increased RTE cells
51
What is normal flora and where is it found?
- Candida species - GI tract and vagina - normal bacteria flora keep in control
52
What causes yeasts to proliferate
Antibiotics, pH change, increased glucose in urine
53
Cause of kidney failure
Failure of kidneys to maintain adequate excretory, regulatory and endocrine function. Mechanism: prerenal, renal, postrenal
54
Kidney failure results in
- Decrease in GFR and oliguria - increased nitrogenous concentrations (azotemia) - disturbance of fluid, acid-base and electrolyte - miss of up to 85% nephron function
55
Chronic renal failure leads to
End stage kidney disease, require dialysis or kidney transplant
56
What is renal lithasis
Kidney stones: - calculi, solid aggregates of mineral salts, form within the kidney - calcium base most frequent at 75% - triple phosphates, uric acid and cystine at 23%
57
Factors for formation of renal lithiasis (kidney stones)
- Increase in concentrations of chemical salts - changes in urinary pH - urinary stasis - nucleation or initial crystal formation
58
Clinical findings of renal lithiasis (kidney stones)
Severe pain radiating from lower back to legs; hematuria present in most cases - small stones can be passed - larger stones require lithotripsy or surgery
59
Types of kidney stones
Cystine, calcium, uric acid, struvite
60
Cystine stone
61
Calcium stones
62
Uric acid stones
63
Struvite stones

CLS 304 (8 decks)

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